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Syndrome X (syndrome + x)
Kinds of Syndrome X Selected AbstractsChanges in platelet receptor expression and leukocyte,platelet aggregate formation following exercise in Cardiac Syndrome XJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 7 2006G. A. LANZA No abstract is available for this article. [source] PPAR, and the thiazolidinediones: molecular basis for a treatment of ,Syndrome X'?DIABETES OBESITY & METABOLISM, Issue 4 2002C. Sewter First page of article [source] The metabolic syndrome: evolving evidence that thiazolidinediones provide rational therapyDIABETES OBESITY & METABOLISM, Issue 4 2006Kathleen L. Wyne The metabolic syndrome, also known as the dysmetabolic syndrome, syndrome X or the insulin resistance syndrome, refers to the clustering of cardiovascular disease risk factors that are present in many individuals who are at increased risk for both cardiovascular events and type 2 diabetes. Prediabetic subjects typically exhibit an atherogenic pattern of cardiovascular risks that is associated with hyperinsulinaemia. Thus, identification of components of the metabolic syndrome is important if patients are to be treated early enough to prevent cardiovascular events and other complications related to diabetes. Therapies targeted to specific components of the metabolic syndrome such as improving glycaemic control, managing dyslipidaemia and reducing the prothrombotic state should help to minimize cardiovascular risk, particularly if initiated early. Traditional pharmacologic agents used to manage the individual components of the metabolic syndrome do not typically impact the other components. The thiazolidinediones, a new class of agents that improve insulin resistance, have the ability, in addition to their glucose-lowering effects, to exert several powerful anti-atherogenic properties, including anti-inflammatory effects in the vascular endothelium, redistribution of visceral fat and reduction of insulin resistance, hyperinsulinaemia and hyperproinsulinaemia. This makes the thiazolidinediones ideal candidates for the early treatment of many components associated with the metabolic syndrome. [source] Plasma matrix metalloproteinase-3 level is an independent prognostic factor in stable coronary artery diseaseEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 9 2005T. C. Wu Abstract Background, Recent evidence suggests the important role of matrix metalloproteinases (MMPs) in the progression of atherosclerosis and development of clinical events. We assessed the prognostic value of different plasma MMPs in patients with stable coronary artery disease (CAD). Materials and methods, A total of 165 consecutive nondiabetic patients with angiographically significant CAD (n = 150) or normal coronary angiograms despite exercise-induced myocardial ischemia (cardiac syndrome X, n = 15) and 17 normal subjects were evaluated. In each subject, plasma inflammatory markers including high sensitivity C-reactive protein (hsCRP) and MMP-2, 3 and 9 were measured. In CAD patients, major cardiovascular events including cardiac death, nonfatal myocardial infarction, unscheduled coronary revascularization and hospitalization as a result of unstable angina were prospectively followed up for more than 6 months. Results, Plasma levels of MMPs were significantly higher in CAD patients than in those with cardiac syndrome X and in normal subjects (MMP-2: 914·76 ± 13·20 vs. 830·79 ± 31·95 vs. 783·08 ± 28·40 ng mL,1, P = 0·002; MMP-3: 129·59 ± 4·21 vs. 116·86 ± 8·09 vs. 91·71 ± 9·55 ng mL,1, P = 0·011; MMP-9: 31·42 ± 2·84 vs. 11·40 ± 5·49 vs. 6·71 ± 2·89 ng mL,1, P = 0·006). In CAD patients, there were 48 major cardiovascular events during a mean follow-up period of 17·74 ± 0·85 months. The numbers of diseased vessels (HR = 2·19, 95% CI 1·20,1·02, P = 0·011), plasma hsCRP (HR = 2·21, 95% CI 1·18,4·11, P = 0·013) and MMP-3 level (HR = 2·46, 95% CI = 1·15,5·28, P = 0·021) were associated with the development of cardiovascular events. However, only the plasma MMP-3 level was an independent predictor of the adverse events in CAD patients (HR = 2·47, 95% CI 1·10,5·54, P = 0·028). Conclusions, Plasma MMP levels were increased in CAD patients. Plasma MMP-3 level, rather than hsCRP, was an independent prognostic marker for future cardiovascular events, suggesting its potential role in risk stratification and clinical management of stable CAD. [source] Autogenic training reduces symptom frequency in women with cardiac syndrome XFOCUS ON ALTERNATIVE AND COMPLEMENTARY THERAPIES AN EVIDENCE-BASED APPROACH, Issue 3 2009Article first published online: 3 JUN 2010 [source] Imbalance of plasma membrane ion leak and pump relationship as a new aetiological basis of certain disease statesJOURNAL OF INTERNAL MEDICINE, Issue 6 2003G. Ronquist Abstract. The basis for life is the ability of the cell to maintain ion gradients across biological membranes. Such gradients are created by specific membrane-bound ion pumps [adenosine triphosphatases (ATPases)]. According to physicochemical rules passive forces equilibrate (dissipate) ion gradients. The cholesterol/phospholipid ratio of the membrane and the degree of saturation of phospholipid fatty acids are important factors for membrane molecular order and herewith a determinant of the degree of non-specific membrane leakiness. Other operative principles, i.e. specific ion channels can be opened and closed according to mechanisms that are specific to the cell. Certain compounds called ionophores can be integrated in the plasma membrane and permit specific inorganic ions to pass. Irrespective of which mechanism ions leak across the plasma membrane the homeostasis may be kept by increasing ion pumping (ATPase activity) in an attempt to restore the physiological ion gradient. The energy source for this work seems to be glycolytically derived ATP formation. Thus an increase in ion pumping is reflected by increased ATP hydrolysis and rate of glycolysis. This can be measured as an accumulation of breakdown products of ATP and end-products of anaerobic glycolysis (lactate). In certain disease entities, the balance between ATP formation and ion pumping may be disordered resulting in a decrease in inter alia (i.a.) cellular energy charge, and an increase in lactate formation and catabolites of adenylates. Cardiac syndrome X is proposed to be due to an excessive leakage of potassium ions, leading to electrocardiographic (ECG) changes, abnormal Tl-scintigraphy of the heart and anginal pain (induced by adenosine). Cocksackie B3 infections, a common agent in myocarditis might also induce an ionophore-like effect. Moreover, Alzheimer's disease is characterized by the formation of extracellular amyloid deposits in the brain of patients. Perturbation of cellular membranes by the amyloid peptide during the development of Alzheimer's disease is one of several mechanisms proposed to account for the toxicity of this peptide on neuronal membranes. We have studied the effects of the peptide and fragments thereof on 45Ca2+ -uptake in human erythrocytes and the energetic consequences. Treatment of erythrocytes with the ,1,40 peptide, results in qualitatively similar nucleotide pattern and decrease of energy charge as the treatment with Ca2+ -ionophore A23187. Finally, in recent studies we have revealed and published in this journal that a rare condition, Tarui's disease or glycogenosis type VII, primarily associated with a defect M-subunit of phosphofructokinase, demonstrates as a cophenomenon an increased leak of Ca2+ into erythrocytes. [source] Altered body composition in preterm infants at hospital dischargeACTA PAEDIATRICA, Issue 8 2009Richard J Cooke Abstract Aim:, To test the hypotheses that body size is reduced and body composition altered in preterm infants at hospital discharge. Methods:, Preterm infants (,34 weeks gestation, ,1750 g at birth) were enrolled. Body weight, length and head circumference were converted to standard deviation or z- scores. Body composition was measured using dual emission X-ray absorptiometry. The results were analysed using standard statistics. Results:, One hundred and forty-nine infants (birth weight = 1406 ± 248 g, gestation = 31 ± 1.7 weeks) were studied. Postmenstrual age at discharge was 37 ± 1.2 weeks. Z -scores for head circumference, weight and length differed (,0.1 ± 0.6 > ,1.4 ± 0.6 > ,1.9 ± 0.6; p < 0.0001). Global fat-free mass was less in study infants than the reference infant at the same weight (2062 < 2252 g; p < 0.0001) or gestation (2062 < 2667 g; p < 0.0001). Global fat mass was greater in study infants than the reference infant at the same weight (307 > 198 g, 13 > 8%) or gestation (307 > 273 g; 13 > 9%; p < 0.0001). Changes in central fat mass closely paralleled those in global fat mass (r2 = 0.76, p < 0.0001). Conclusion:, Reduced linear growth and a reduced fat-free mass suggest that dietary protein needs were not met before discharge. A reduced fat-free mass coupled with an increased global and central fat mass echoes concerns about the development of insulin resistance and metabolic syndrome X in these high-risk infants. [source] Vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 serum level in patients with chest pain and normal coronary arteries (syndrome X)CLINICAL CARDIOLOGY, Issue 4 2001Dimitris Tousoulis M.D., Ph.D. Abstract Background: Plasma levels of soluble vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (IC AM-1) mediators of leukocyte adhesion to vascular endothelium may implicate in the pathogenesis of the syndrome of chest pain with normal coronary arteries. Hypothesis: We attempted to determine whether markers of endothelial activation are raised in patients with chest pain and normal coronary arteries. Methods: We measured plasma VCAM-1, ICAM-1 (ng/ml) in 36 patients (34 men, 2 women, aged 62 ± 9 years) with stable angina, coronary artery disease (CAD), and a positive response to exercise test; in 21 patients (6 men, 15 women, aged 56 ± 9 years) with chest pain and normal coronary arteriograms (syndrome X); and in 11 healthy control subjects (8 men, 3 women, aged 49 ± 14 years). Results: Plasma ICAM-1 levels were significantly higher both in patients with CAD (mean ± standard error of the mean) (328 ± 26, p<0.05), and in syndrome X (362 ± 22, p<0.01) than in controls (225 ± 29). VCAM-1 levels were also higher in syndrome X (656 ± 42 ng/ml) and in patients with CAD (626 ± 42 ng/ml) than in controls (551 ± 60, p=0.09). Conclusions: ICAM-1 and VCAM-1 levels are increased both in patients with CAD and with syndrome X compared with control individuals. These findings may suggest the presence of chronic inflammation with involvement of the endothelium in patients with anginal chest pain and normal coronary angiograms. [source] | ||||||||||